SLEEP DISORDERED BREATHING INTRODUCTION IN OBSTRUCTIVE SLEEP APNEA (OSA), REPETITIVE COL- LAPSE OF THE UPPER AIRWAY DURING SLEEP RESULTS IN MULTIPLE EPISODES OF HYPOXEMIA AND subsequent repetitive arousals

IN OBSTRUCTIVE SLEEP APNEA (OSA), REPETITIVE COLLAPSE OF THE UPPER AIRWAY DURING SLEEP RESULTS IN MULTIPLE EPISODES OF HYPOXEMIA AND subsequent repetitive arousals that fragment sleep. These events and the associated autonomic and neurohumoral disturbances are considered to lead to the many symptoms and signs of OSA and contribute to the long-term morbidity.1,2 The repetitive arousals are a dominant mechanism causing excessive daytime sleepiness. However, the increases in drive to the inspiratory muscles and the work of breathing during apneas and hypopneas may cause more-subtle symptoms and effects on neural control mechanisms for both respiratory and upper airway muscles. Upper airway patency is dependent on the balance between the tendency of the airway to collapse, induced by the subatmospheric intraluminal pressure during inspiration, and upper airway dilator muscle activity and intrinsic passive properties. Upper airway negative pressure is the key force provoking airway occlusion during sleep and is related to airflow and the cross-sectional area of the airway. In healthy control subjects, a transient negative pressure causes a reflex increase in upper airway dilator muscle activity.3-6 This is mediated by mechanoreceptors in the upper airway sensitive to changes in airway pressure3,4,7 and proprioceptive afferents in the tongue.8 This reflex is significantly attenuated in non-rapid eye movement sleep in healthy subjects6,9,10 and is not sufficient to maintain airway patency during sleep.11 In people with OSA, this reflex is not attenuated, compared with control subjects, during wakefulness12 and probably also not during sleep.13,14 However, upper airway muscle activity is reduced relatively more in OSA patients during sleep than in control subjects,13 and this probably contributes to more-frequent airway collapse. The current study examined the reflex responses of the inspiratory pump muscles to brief airway occlusion in patients with OSA of varying severity and a control group of healthy subjects. The brief airway occlusion causes a sudden loading of the inspiratory muscles and a sudden decrease in airway pressure. This situation is functionally equivalent to the stretch reflex or loading reflex seen in limb muscles. A short-latency inhibitory reflex response is generated in inspiratory muscles, in response to airway occlusion,15,16 opposite in direction to the reflex facilitation of upper airway dilator muscles in response to negative pressure. Previous studies have shown that the inhibitory response to airway occlusion in inspiratory pump muscles is likely to be mediated by inspiratory muscle afferents.15,17 However, this does not imply that airway receptors cannot influence the reflex response. The initial inhibitory response to loading, which may be an important protective reflex to prevent aspiration,15 is of interest because the equivalent response in limb muscles (stretch reflex) usually consists of 2 phases of excitation with no intervening inhibition.18-21 This suggests that there is a functionally different organization of the reflex pathways for inspiratory, compared with limb, muscles, perhaps to allow for integration with airway and chemoreceptor signals at the level of the medulla. In subjects with asthma, the inhibitory reflex is prolonged, compared with nonasthmatic subjects, possibly because they experience chronically increased airway resistance, which intermittently loads their inspiratory muscles.22 We hypothesized that the Brief Airway Occlusion Produces Prolonged Reflex Inhibition of Inspiratory Muscles in Obstructive Sleep Apnea